L5- Pulmonary Pathology III Flashcards
what are the 2 ways to classify Asthma
- based on prior sensitization to allergen: atopic, non-atopic
- based on triggers: drugs, occupational, environmental, seasonal, exercise
Atopic Asthma:
(1) mechanism
(2) triggers
(3) age of onset
(4) FHx
(5) skin tests
(6) PMHx
1- type I hypersensitivity, IgE 2- environmental: dust, pollen, dander, food 3- childhood 4- yes, FHx present 5- immeadiate wheal and flare 6- allergic rhinitis, eczema
Non-atopic Asthma:
(1) mechanism
(2) triggers
(3) age of onset
(4) FHx
(5) skin tests
(6) PMHx
1- bronchial hyper-irritability
2- viral respiratory infections, SO2, NO2, etc
3- less common, begins anytime
4- less common to have FHx
5- no skin test results
6- less common to have certain PMHx components
Atopic asthma is a (1) type of reaction or body response. The (2) will be inhaled and elicit a response from (3) cells in (4) type people. (3) will release the following, (5), in order to cause (6).
1- type I hypersensitivity (IgE mediated) 2- allergen 3- TH2 cells 4- genetically predisposed individuals 5- IL-4, IL-5, IL-13 6- IgE mediated mast cell degranulation
list the 3 most important CKs in Atopic Asthma pathogenesis, include their functions
(type I hypersensitivity reaction, IgE mediated, all released from TH2 cells)
- IL-4: stimulates IgE production
- IL-5: activates eosinophils
- IL-13: stimulates mucus production + promotes IgE production from B-cells
All are used in order to promote IgE coating of mast cells => degranulation
atopic asthma pathogenesis is split into (1) which presents at (2) time, and then (3) presenting at (4) time; this phenomenon is due to (5)
1/2- early phase, minutes
3/4- late phase, 4-24 hrs
5- two separate waves of mediators
describe the components of the early phase of Atopic Asthma pathogenesis
(1st wave of mast cell degranulation, initiates in minutes)
- bronchoconstriction (direct vagal nerve stimulation)
- inc mucus production
- vasodilation => inc permeability
- further leukocyte recruitment
describe the components of the late phase of Atopic Asthma pathogenesis
(2nd wave of mast cell degranulation, initiates 4-24 hrs later)
- activation of eosinophils, PMNs, T-cells
- epithelial activation –> TH2 cell and eosinophil recruitment
Non-atopic asthma is usually caused by (1) and or (2). (1) will induce (3) which in turn will (4) in response to (2). (5) and (6) are critical similarities to atopic asthma.
1- secondary to viral infections 2- inhaled irritants: SO2, NO2, O3 3- virus induced mucosal damage 4- lower threshold of sub epithelial vagal receptors 5- inflammatory mediators 6- Tx
(1) is the most common drug observed in drug-induced asthma. This results from (1) inhibiting (2) production and therefore increasing (3) production which are responsible for the asthma reaction, specifically (4). This will present as (5) clinically.
1- aspirin 2- TXs, PGs (dec) 3- LTs (inc) 4- LT mediated bronchoconstriction 5- recurrent rhinitis, nasal polyps, urticaria, bronchospasm
list common triggers found in Occupational Asthma
fumes, organic dusts, chemical dusts, gases: epoxy resins / plastics, wood, cotton, platinum, toluene
*note- asthma attacks follow repeated exposure
list the 2 main features of the gross appearance of asthma
- occlusion of airways by thick mucus
- lung hyperinflation (due to obstruction)
Asthma Histology:
- (1) fluid changes
- (2) epithelial changes
- (3) observed in bronchial lumen
- inc in total (4) cells
- inflammation => inc (5) cells
- (6) changes to bronchial smooth muscle cells
- (7) changes to basement membrane
1- edema
2- patchy necrosis
3- mucus plugs with Curschmann spirals, Charcot Leyden crystals, eosinophils
4- goblet cells
5- eosinophils
6- SM hypertrophy and hyperplasia
7- thickened BM // sub-basement membrane fibrosis
define:
(1) Curschmann spirals
(2) Charcot Leyden crystals
1- whorls of shed epithelium (necrotic cells)
2- collections of crystalloids formed by Protein Galactin-10 via eosinophils
Asthma is defined as (1- include Sxs + its frequency) clinically. (2) is progressively trapped in lung because of (3). Attacks are considered (4) and last for (5).
1- recurrent sudden attacks of dyspnea, chest tightness, expiratory wheezing/ronchi, cough with thick sputum
2- air –> progressive hyperinflation
3- (air trapped distal to) mucus plug in bronchi
4- episodic (nights, early mornings)
5- hrs, subsiding spontaneously or with therapy
define status asthmaticus
- severe, prolonged asthma attack
- non-responsive to therapy
- NEEDS emergency management
Physical Exam for Asthma:
- (1) RR change
- (2) on auscultation
- (3) spirometry changes
1- tachypnea
2- expiratory (mostly) wheeze –> indicates obstruction
3- FEV1 <30%, inc all lung volumes, dec FEV1:FVC
Laboratory Analysis for Asthma:
- (1) seen in serum
- (2) seen on ABG
- (3) seen in sputum
1- eosinophilia
2- hypoxia, hypercapnia, respiratory acidosis
3- Curschmann spirals, Chracot Leyden crystals, eosinophils